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Conditional inactivation of Tgfbr2 in cranial neural crest causes cleft palate and calvaria defects
Cleft palate and skull malformations represent some of the most frequent congenital birth defects in the human population. Previous studies have shown that TGFβ signaling regulates the fate of theExpand
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Medial edge epithelium fate traced by cell lineage analysis during epithelial-mesenchymal transformation in vivo.
Vital cell labeling techniques were used to trace the fate of the medial edge epithelial (MEE) cells during palatal fusion in vivo. Mouse palatal tissues were labeled in utero with DiI. The fetusesExpand
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Oral bisphosphonate use and the prevalence of osteonecrosis of the jaw: an institutional inquiry.
BACKGROUND Initial reports of osteonecrosis of the jaw (ONJ) secondary to bisphosphonate (BP) therapy indicated that patients receiving BPs orally were at a negligible risk of developing ONJ comparedExpand
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Multicentric peripheral ossifying fibroma.
Peripheral ossifying fibroma (POF) is a common solitary gingival growth thought to arise from the periodontal ligament. Though the etiology of POF remains unknown, some investigators consider it anExpand
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Identification of microbial biofilms in osteonecrosis of the jaws secondary to bisphosphonate therapy.
PURPOSE Biofilm theory has emerged to explain the etiology of the chronic infections that have come to constitute between 65% to 80% of the microbial diseases treated by physicians in the developedExpand
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Caiman periodontium as an intermediate between basal vertebrate ankylosis‐type attachment and mammalian “true” periodontium
The teeth of many fish, amphibia, and reptiles are attached to the alveolar bone via ankylosis. In contrast, mammalian periodontia are characterized by a gomphosis, an attachment of the tooth root inExpand
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TGF‐β3–dependent SMAD2 phosphorylation and inhibition of MEE proliferation during palatal fusion
  • X. Cui, Y. Chai, +4 authors C. Shuler
  • Biology, Medicine
  • Developmental dynamics : an official publication…
  • 1 July 2003
Transforming growth factor (TGF) ‐β3 is known to selectively regulate the disappearance of murine medial edge epithelium (MEE) during palatal fusion. Previous studies suggested that the selectiveExpand
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Overexpression of Smad2 in Tgf-beta3-null mutant mice rescues cleft palate.
Transforming growth factor (TGF)-beta3 is an important contributor to the regulation of medial edge epithelium (MEE) disappearance during palatal fusion. SMAD2 phosphorylation in the MEE has beenExpand
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Epidermal growth factor receptor function is necessary for normal craniofacial development and palate closure
Craniofacial malformations are among the most frequent congenital birth defects in humans; cleft palate, that is inadequate fusion of the palatal shelves, occurs with an annual incidence of 1 in 700Expand
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Transforming growth factor‐β3 regulates transdifferentiation of medial edge epithelium during palatal fusion and associated degradation of the basement membrane
Studies on transforming growth factor β3 (TGF‐β3) deficient mice have shown that TGF‐β3 plays a critical role in palatogenesis. These null mutant mice have clefting of the secondary palate, caused byExpand
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